Etiology of Anal Fissures
Anal fissures result from a combination of mechanical trauma to the anoderm and internal anal sphincter hypertonia that creates local ischemia, perpetuating a vicious cycle of pain, spasm, and impaired healing. 1, 2
Primary Etiologic Mechanisms
Mechanical Trauma
- The initial lesion is a tear in the anoderm caused by overstretching of the anal canal, most commonly from passage of hard stools 3
- Contrary to common belief, less than 25% of patients with anal fissures actually complain of constipation, indicating that hard stool passage alone is insufficient to explain fissure development 1
- Diarrhea and irritation from loose stools can also cause anorectal trauma leading to fissure formation 4
- Prior anorectal surgery may traumatize the anoderm and precipitate fissure development 4, 3
Internal Anal Sphincter Hypertonia and Ischemia
- Internal anal sphincter hypertonia is strongly correlated with decreased anodermal vascular blood flow, creating an ischemic environment that prevents healing 1, 2
- Resting anal pressure in fissure patients averages approximately 114 ± 17 cm H₂O, markedly higher than the normal average of approximately 73 ± 27 cm H₂O 2
- The internal anal sphincter (IAS), not the external sphincter, generates the painful spasm and elevated resting pressure that perpetuates the fissure 2
- This creates a vicious cycle: the fissure causes pain → pain triggers sphincter spasm → spasm reduces blood flow → ischemia prevents healing → persistent fissure 3
Anatomical Distribution and Its Etiologic Significance
- Approximately 90% of typical anal fissures occur posteriorly in the midline, with the remainder occurring anteriorly 1
- Anterior midline fissures occur in approximately 10% of women versus only 1% of men 1
- The posterior midline location reflects the relatively poor vascular supply and mechanical stress concentration in this area during defecation 1
Atypical Fissures: Secondary Etiologies
Fissures located off the midline (lateral or multiple) indicate underlying systemic disease and require urgent evaluation before treatment. 1, 2
Inflammatory Bowel Disease
- Crohn's disease is a common cause of atypical fissures, with perianal fistulae occurring in 13% to 27% of CD patients 5
- Perianal fistulae may be the initial manifestation of Crohn's disease in up to 81% of patients who develop perianal disease 5
- Ulcerative colitis can also present with atypical fissures 2
Infectious Etiologies
- HIV/AIDS can cause atypical fissures through direct infection or opportunistic pathogens 1, 2
- Syphilis, herpes, tuberculosis, and actinomycosis are all recognized infectious causes 5, 1
Malignancy
- Anorectal cancer can present as an atypical fissure 1, 2
- Leukemia has been associated with atypical fissure formation 1
Other Secondary Causes
- Radiation proctitis following pelvic radiation therapy 5
- Foreign body trauma 5
- Prior anal surgery 5, 3
Pathophysiologic Evolution
Acute to Chronic Progression
- Acute fissures are superficial tears that may heal spontaneously in approximately 50% of cases within 10-14 days with conservative management 1, 6
- When the pain-spasm-ischemia cycle is not interrupted, the fissure becomes chronic (>8 weeks duration) 2
- Chronic fissures develop signs of chronicity including a sentinel skin tag distally, hypertrophied anal papilla proximally, visible internal sphincter muscle at the fissure base, and fibrosis 1
The Multifactorial Nature
- The exact etiology remains incompletely understood and represents a multifactorial process rather than a single causative mechanism 1, 7
- The interplay between mechanical trauma, sphincter hypertonia, and ischemia creates a self-perpetuating condition 4, 8
Critical Clinical Pitfalls
- Do not assume all anal fissures are caused by constipation—the majority of patients do not report hard stools as a primary complaint 1
- Never dismiss an off-midline or lateral fissure as "typical"—these locations mandate urgent evaluation for IBD, infection, or malignancy before initiating standard therapy 1, 2
- Recognize that diarrhea is an equally important etiologic factor and must be addressed before surgical intervention to avoid incontinence 6